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Title: MAD2-p31comet axis deficiency reduces cell proliferation, migration and sensitivity of microtubule-interfering agents in glioma

Journal Article · · Biochemical and Biophysical Research Communications
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  1. Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237 (China)
  2. Department of Neurosurgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000 (China)
  3. Department of Neurology, Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001 (China)

Mitotic arrest deficient-like-1 (MAD2, also known as MAD2L1) is thought to be an important spindle assembly checkpoint protein, which ensures accurate chromosome segregation and is closely associated with poor prognosis in many cancer. As a MAD2 binding protein, p31{sup comet} counteracts the function of MAD2 and leads to mitotic checkpoint silence. In this study, we explore the function of MAD2-p31{sup comet} axis in malignant glioma cells. Our results showed that disruption of MAD2-p31{sup comet} axis by MAD2 knockdown or p31{sup comet} overexpression suppressed cell proliferation, survival and migration of glioma, indicating that MAD2-p31{sup comet} axis is required for maintaining glioma cells malignancy. It is noted that MAD2 depletion or p31{sup comet} overexpression reduced the sensitivity of glioma cells to microtubule-interfering agents paclitaxel and vinblastine, providing clinical guidance for application of such drugs. Taken together, our findings suggest that MAD2-p31{sup comet} axis may serve as a potential therapeutic target for glioma.

OSTI ID:
23137260
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 498, Issue 1; Other Information: Copyright (c) 2018 Published by Elsevier Inc.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English